Differential down-regulation of voltage-gated calcium channel currents by glutamate and BDNF in embryonic cortical neurons

Autor: Sylvie Boisseau, Michel De Waard, Alexandre Bouron, Leticia Peris
Přispěvatelé: Laboratoire de biophysique moléculaire et cellulaire (LBMC), Université Joseph Fourier - Grenoble 1 (UJF)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Centre National de la Recherche Scientifique (CNRS), Canaux calciques , fonctions et pathologies, Université Joseph Fourier - Grenoble 1 (UJF)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Organisation Fonctionnelle du Cytosquelette, Université Joseph Fourier - Grenoble 1 (UJF)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR27, We also wish to thank the Fondation pour la Recherche Me´dicale for financial support., Centre National de la Recherche Scientifique (CNRS)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Joseph Fourier - Grenoble 1 (UJF), Andrieux, Annie
Jazyk: angličtina
Rok vydání: 2006
Předmět:
MESH: Neurons
MESH: Calcium Channel Blockers
Tropomyosin receptor kinase B
MESH: Brain-Derived Neurotrophic Factor
MESH: Down-Regulation
Transient receptor potential channel
chemistry.chemical_compound
0302 clinical medicine
Neurotrophic factors
calcium channels
Excitatory Amino Acid Agonists
MESH: Animals
TRPC
Cells
Cultured
Neurons
0303 health sciences
Voltage-dependent calcium channel
General Neuroscience
MESH: Receptor
trkB
Glutamate receptor
Imidazoles
MESH: Glutamic Acid
MESH: Neuroprotective Agents
Calcium Channel Blockers
Neuroprotective Agents
MESH: Calcium
MESH: Calcium Channels
NMDA receptor
cerebral cortex
[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
MESH: Imidazoles
MESH: Cells
Cultured
mice
Down-Regulation
Glutamic Acid
glutamate
Biology
MESH: Calcium Signaling
03 medical and health sciences
BAPTA
MESH: Mice
Inbred C57BL
[SDV.BBM] Life Sciences [q-bio]/Biochemistry
Molecular Biology
Animals
Receptor
trkB
[SDV.BBM]Life Sciences [q-bio]/Biochemistry
Molecular Biology
Calcium Signaling
[SDV.NEU] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]
MESH: TRPC Cation Channels
MESH: Mice
030304 developmental biology
TRPC Cation Channels
Brain-Derived Neurotrophic Factor
MESH: Cerebral Cortex
Mice
Inbred C57BL
MESH: Cytoprotection
BDNF
chemistry
nervous system
Cytoprotection
Calcium
MESH: Excitatory Amino Acid Agonists
Neuroscience
030217 neurology & neurosurgery
Zdroj: European Journal of Neuroscience
European Journal of Neuroscience, 2006, 24 (3), pp.699-708. ⟨10.1111/j.1460-9568.2006.04946.x⟩
European Journal of Neuroscience, Wiley, 2006, 24 (3), pp.699-708. ⟨10.1111/j.1460-9568.2006.04946.x⟩
ISSN: 0953-816X
1460-9568
DOI: 10.1111/j.1460-9568.2006.04946.x⟩
Popis: International audience; In the embryonic brain, post-mitotic cortical neurons migrate from their place of origin to their final location. Various external factors such as hormones, neurotransmitters or peptides regulate their migration. To date, however, only a few studies have investigated the effects of these external factors on the electrical properties of the newly formed embryonic cortical neurons. The aim of the present study was to determine whether glutamate and brain-derived neurotrophic factor (BDNF), known to regulate neuronal cell migration, could modulate currents through voltage-gated calcium channels (ICa) in cortical neurons isolated from embryonic day 13 (E13) mouse foetuses. Whole cell recordings of ICa showed that E13 cortical cells kept 1 day in vitro expressed functional low- and high-voltage activated (LVA and HVA) Ca2+ channels of T-, L- and N-types. A 1-day glutamate treatment non-specifically inhibited LVA and HVA ICa whereas BDNF down-regulated HVA with N-type ICa being more depressed than L-type ICa. The glutamate-induced ICa inhibition was mimicked by NMDA. BDNF exerted its action by recruiting trkB receptors and SKF-96365-sensitive channels. BAPTA prevented the glutamate- and the BDNF-dependent inhibition of Ica, indicating a Ca2+-dependent mechanism of action. It is proposed that an influx of Ca2+ through NMDA receptors depresses the expression of LVA and HVA Ca2+ channels whereas a Ca2+ influx through SKF-96365-sensitive TRPC (transient receptor potential protein of C subtype) channels preferentially inhibits the expression of HVA Ca2+ channels. Glutamate and BDNF appear as potent modulators of the electrical properties of early post-mitotic neurons. By down-regulating ICa they could exert a neuroprotective action on embryonic cortical neurons.
Databáze: OpenAIRE
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